There are many arrhythmias which can occur to affect the ability of the heart to effectively pump blood. In a normal heart, a stimulating pulse originates at the sinus node and is conducted throughout the heart by various conductive bundles causing sequential atrial and ventricular contractions to pump blood through the heart. One form of arrhythmia involves a complete blockage of the normal conductive paths whereby the exciting pulse is blocked from reaching a portion of the heart to cause a contraction. Implanted cardiac pacers have long been available to detect such a heart blockage and provide a substitute stimulating pulse at a location which avoids the blockage.
Yet another arrhythmia with serious consequences is tachycardia, a condition where an abnormally high heart beat rate occurs. Tachycardia severly affects the ability of the heart to pump blood and the higher the heart beat rate, the more dangerous the condition.
There are many mechanisms which have been postulated as the cause of a tachycardia. A first mechanism is abnormal automaticity which involves a basic malfunction of heart tissue. The present invention does not concern this basic malfunction.
A second cause of tachycardia involves a rapidly circulating impulse in a circus pathway. This condition is typically called reentry tachycardia. In general, a reentry path may be established when a normal pathway is blocked while alternate pathways remain conducting. If the conduction velocity of the pathway and the refractory period of the heart tissue obtain a critical relationship, a reentry tachycardia may be initiated.
During the refractory period, the heart muscle is insensitive and will not respond to an arriving signal. However, a response may be obtained as soon as the muscle has recovered. Accordingly, if the signal completes its circus movement as the muscle concludes the refractory period, a reentry path is established and a condition of tachycardia now exists. Heartbeat rates of well over 200/minute are not uncommon.
It has been found that a tachycardia based upon reentry may be stopped by refractory tissue in the reentry pathway. Stimulating pulses may be introduced to the heart to create refractoriness ahead of the circulating impulse. As hereinbelow discussed, it is known that the arrival of a single stimulating pulse at a critical moment may terminate the tachycardia. Where a single pulse is not effective, two or more stimulating pulses may be introduced. A first pulse creates an area of tissue in a refractory period around the site of the stimulation. A second pulse applied at the stimulation site can then be applied at an interval effective to produce refractory tissue ahead of the circulating impulse.